Amoebae As Host Models To Study The Interaction With Pathogens
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Amoebae as Host Models to Study the Interaction with Pathogens
The human body is constantly faced with microorganisms. Most of these bacteria, fungi, and viruses are harmless, many of them are beneficial, and a small fraction is pathogenic. For humans, infection with pathogenic microorganisms can be very serious or even fatal, ranging from mild transient or chronic infections to death. The first line of defence against pathogens is our innate immune system. Beside chemical and physical defence mechanisms of the innate immune system, phagocytic cells such as macrophages play a crucial role in the fight against pathogenic microorganisms. However, phagocytic cells and pathogens are in a constant evolutionary arms race, inventing new strategies to successfully kill pathogens and learning how to resist phagocytosis and intracellular killing, respectively. If pathogens are not obligatory adapted to the human body or other animals, they also have to face environmental phagocytes in the form of amoebae. Many aspects of phagocytosis and intracellular killing are surprisingly well conserved between amoebae and macrophages. Therefore, pathogens that have evolved with environmental amoebae as their “training grounds” can also be successful during infection of macrophages and other animal phagocytic cells. In this Research Topic, we provide the latest knowledge about the potential of using amoebae as host models to study the interaction with pathogens. The Research Topic covers the interaction of amoebae with bacteria, fungi, and viruses and also illustrates the similarities and differences between amoebae and macrophages. Investigation of evolutionary conserved pathways of amoebae and macrophages furthers our understanding of the biology of host-pathogen interactions and helps to develop new anti-infection therapies.
Model Organisms for Microbial Pathogenesis, Biofilm Formation and Antimicrobial Drug Discovery
This book provides essential insights into microbial pathogenesis, host-pathogen interactions, and the anti-microbial drug resistance of various human pathogens on the basis of various model organisms. The initial sections of the book introduce readers to the mechanisms of microbial pathogenesis, host-pathogen interactions, anti-microbial drug resistance, and the dynamics of biofilm formation. Due to the emergence of various microbial resistant strains, it is especially important to understand the prognosis for microbial infections, disease progression profiles, and mechanisms of resistance to antibiotic therapy in order to develop novel therapeutic strategies. In turn, the second part of the book presents a comparative analysis of various animal models to help readers understand microbial pathogenesis, host-pathogen interactions, anti-microbial drug discovery, anti-biofilm therapeutics, and treatment regimes. Given its scope, the book represents a valuable asset for microbiologists, biotechnologists, medical professionals, drug development researchers, and pharmacologists alike.
The Mononuclear Phagocyte System in Infectious Disease
Author: Geanncarlo Lugo-Villarino
language: en
Publisher: Frontiers Media SA
Release Date: 2019-10-04
The Mononuclear Phagocyte System (MPS) of vertebrates is composed of monocytes, macrophages and dendritic cells. Together, they form part of the first line of immune defense against a variety of pathogens (bacteria, fungi, parasites and viruses), and thus play an important role in maintaining organism homeostasis. The mode of transmission, type of replication and mechanism of disease-causing differ significantly for each pathogen, eliciting a unique immune response in the host. Within this context, the MPS acts as both the sentinel and tailor of the immune system. As sentinels, MPS cells are found in blood and within tissues throughout the body to patrol against pathogenic insult. The strategy to detect 'microbial non-self' relies on MPS to recognize conserved microbial products known as 'pathogen-associated molecular pattern' (PAMPs). PAMPs recognition represents a checkpoint in the response to pathogens and relies on conserved 'pattern recognition receptors' (PRRs). Upon PRR engagement, MPS mount a cell-autonomous attack that includes the internalization and compartmentalization of intracellular pathogens into toxic compartments that promote destruction. In parallel, MPS cells launch an inflammatory response composed of a cellular arm and soluble factors to control extracellular pathogens. In cases when innate immunity fails to eliminate the invading microbe, MPS serves as a tailor to generate adaptive immunity for pathogen eradication and generation of "memory" cells, thus ensuring enhanced protection against re-infection. Indeed, MPS cell functions comprise the capture, process, migration and delivery of antigenic information to lymphoid organs, where type-1 immunity is tailored against intracellular microbes and type-2 immunity against extracellular pathogens. However, this potent adaptive immunity is also a double-edge sword that can cause aberrant inflammatory disorders, like autoimmunity or chronic inflammation. For this reason, MPS also tailors tolerance immunity against unwanted inflammation. Successful clearance of the microbe results in its destruction and proper collection of debris, resolution of inflammation and tissue healing for which MPS is essential. Reciprocally, as part of the evolutionary process taking place in all organisms, microbes evolved strategies to circumvent the actions bestowed by MPS cells. Multiple pathogens modulate the differentiation, maturation and activation programs of the MPS, as an efficient strategy to avoid a dedicated immune response. Among the most common evasion strategies are the subversion of phagocytosis, inhibition of PRR-mediated immunity, resistance to intracellular killing by reactive oxygen and nitrogen species, restriction of phagosome maturation, modulation of cellular metabolism and nutrient acquisition, regulation of cell death and autophagy, and modulation of pro-inflammatory responses and hijacking of tolerance mechanisms, among others. The tenet of this eBook is that a better understanding of MPS in infection will yield insights for development of therapeutics to enhance antimicrobial processes or dampen detrimental inflammation for the host's benefit. We believe that contributions to this topic will serve as a platform for discussion and debate about relevant issues and themes in this field. Our aim is to bring expert junior and senior scientists to address recent progress, highlight critical knowledge gaps, foment scientific exchange, and establish conceptual frameworks for future MPS investigation in the context of infectious disease.